Richard M. Peek, Jr. MD

I developed expertise in the molecular pathogenesis of H. pylori as a research fellow in the Divisions of Gastroenterology and Infectious Diseases at Vanderbilt in the laboratory of Dr. Martin Blaser. As an independent investigator, our laboratory initially defined mechanisms through which H. pylori cag⁺ strains augment cancer risk- specifically, demonstrating that such strains dissociate epithelial proliferation from apoptosis in vivo. In mechanistic studies, our laboratory subsequently determined that adherence of H. pylori cag⁺ strains to gastric epithelial cells is critical for induction of inflammation and injury. Therefore, the overarching theme for our research has been delineation of the signaling events initiated by bacterial:epithelial cell contact that regulate epithelial cellular phenotypes related to carcinogenesis, particularly malignancies that arise within foci of inflammation. In examining variability of host responses to carcinogenic strains, our laboratory demonstrated that the strain-specific H. pylori protein, CagA, enters epithelial cells and activates ß-catenin dependent signaling. Our laboratory also developed rodent models (Mongolian gerbils and mice) as well as ex vivo gastric gland and organoid culture systems that closely recapitulate cellular organization in the stomach to examine the effects of junctional proteins and ß-catenin on carcinogenic responses to pathogenic H. pylori strains. Recently, we have determined that environmental conditions linked to gastric cancer risk, such as iron deficiency, augment the expression and deployment of microbial virulence constituents and accelerate gastric carcinogenesis. Thus, we have sought to translate results seamlessly from cell culture to rodent models to human populations.

I also have extensive administrative experience. I have served as the Mina Cobb Wallace Professor of Medicine and Cancer Biology and Director of the Division of Gastroenterology, Hepatology and Nutrition at Vanderbilt for the past nine years, during which time the faculty has doubled in size. Our Division is research-driven and work focuses on gastrointestinal malignancies, inflammation and immune dysfunction, microbial pathogenesis, oxidative cellular damage, GI motility disorders, biliary endoscopy, steatohepatitis and hepatocellular carcinoma, gastroesophageal reflux-mediated esophageal diseases, and nutrition. The Division receives approximately $8 million/year in NIH direct funds and has a total research portfolio of over $10 million/year. I direct the Vanderbilt Gastroenterology Training Program (NIH T32) that consolidates Adult and Pediatric GI fellowship and postdoctoral research training at Vanderbilt, and have a vigorous role in mentoring students, residents, fellows and junior faculty. I am also Director of the NIH-funded Vanderbilt Digestive Diseases Research Center, which formally integrates complementary clinical and research programs within Gastroenterology at Vanderbilt.